Evidence map›Paper›PMID 38385073›Full record

ArticleInternational journal of biological sciences2024

Malat1 regulates PMN-MDSC expansion and immunosuppression through p-STAT3 ubiquitination in sepsis.

Yaodong Wang, Caiyan Zhang, Tingyan Liu, Zhenhao Yu, Kexin Wang, Jiayun Ying, Yao Wang, Ting Zhu, Jingjing Li, Xiuchuan Lucas Hu and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Mapping malignant T-cell states and immune circuits in Sézary syndrome by single-cell analysis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Yaodong WangDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Caiyan ZhangDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Tingyan LiuDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Zhenhao YuDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Kexin WangInstitute of Pediatrics, Children's Hospital of Fudan University, National Children's Medical Center, and the Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jiayun YingDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Yao WangDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Ting ZhuDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Jingjing LiShanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.
Xiuchuan Lucas HuLungs for Living Research Centre, UCL Respiratory, University College London, London, UK.
Yufeng ZhouDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Guoping LuDepartment of Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China.
Children's Hospital of Fudan University · CNFudan University · CNNational Health and Family Planning Commission · CNUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) expand during sepsis and contribute to the development of persistent inflammation-immunosuppression-catabolism syndrome. However, the underlying mechanism remains unclear. Exploring the mechanisms of MDSCs generation may provide therapeutic targets for improving immune status in sepsis. Here, a sepsis mouse model is established by cecal ligation and perforation. Bone marrow cells at different sepsis time points are harvested to detect the proportion of MDSCs and search for differentially expressed genes by RNA-sequence. In lethal models of sepsis, polymorphonuclear-MDSCs (PMN-MDSCs) decrease in early but increase and become activated in late sepsis, which is contrary to the expression of metastasis-associated lung adenocarcinoma transcript 1 (Malat1).

Indexed as

Myeloid-Derived Suppressor CellsSepsisAnimalsDisease Models, AnimalImmunosuppression TherapyMiceRNA, Long NoncodingSTAT3 Transcription FactorMalat1 long non-coding RNA, mouseRNA, Long NoncodingStat3 protein, mouseSTAT3 Transcription FactorExperimental sepsisMalat1Polymorphonuclear myeloid-derived suppressor cellSTAT3 pathwayUbiquitination

Identifiers

PMID38385073
PMCPMC10878150
OpenAlexW4391986704

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.